Skip to main content
Fig. 2 | Arthritis Research & Therapy

Fig. 2

From: Senescent skeletal cells cross-talk with synovial cells plays a key role in the pathogenesis of osteoarthritis

Fig. 2

Multiple tissues within the knee contribute to OA progression. Senescent chondrocytes exert a pro-senescence effect on surrounding normal chondrocytes via SASP, and the senescent synovial cells can also act on normal chondrocytes via cytokines such as TNF-α, VEGF, and IL, leading to the cartilage degeneration. The process of subchondral bone degeneration in OA depends on osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Osteoblasts act on osteoclasts via RANKL, which increases their activity accompanied by the secretion of large amounts of calcium-phosphate complex, thus promoting the secretion of MMP-3 and MMP-13 by the chondrocytes which causes cartilage degeneration. On the other hand, osteoblasts can induce subchondral angiogenesis via the TGF-β1/Smad signaling to indirectly induce senescent chondrocytes, which in turn, promote the secretion of more VEGF from the H-type vessel. All of these creating a vicious cycle of senescence and accelerating the development and progression of OA. SASP, senescence-associated secretory phenotype; TNF, tumor necrosis factor; TGFβ, transforming growth factor β; MMP, matrix metalloproteinase; RANKL, receptor activator of nuclear factor κB ligand; VEGF, vascular endothelial growth factor

Back to article page